Sanchez-Bueno A, Greenwood M R, Varela-Nieto I, Marrero I, Gil B, Mato J M, Cobbold P H
Department of Human Anatomy and Cell Biology, University of Liverpool, UK.
Cell Calcium. 1997 Feb;21(2):125-33. doi: 10.1016/s0143-4160(97)90036-1.
Inositol-phosphoglycan (IPG) is a putative mediator of insulin action that has been shown to affect numerous biochemical processes. IPG, prepared from liver membranes, promptly inhibited phenylephrine- or vasopressin-induced [Ca2+]i oscillations when perfused over Fura-2-dextran injected rat hepatocytes. An antibody to IPG suppressed the inhibitory effect of insulin on the [Ca2+]i oscillations. Measurement of the rate of quench of cytoplasmic Fura-2 by extracellular Mn2+ showed that Ca2+ entry occurred continuously in the unstimulated cell and was not affected by phenylephrine or vasopressin. IPG, specifically, almost completely abolished the Mn2+ quench rate. Elevated extracellular [Ca2+] reversed the inhibitory effect of IPG on [Ca2+]i oscillations. We conclude that IPG inhibits the hepatocyte Ca2+ oscillatory by reducing the continuous Ca2+ influx that is required to sustain oscillations in [Ca2+]i.
肌醇磷酸聚糖（IPG）是一种推测的胰岛素作用介质，已被证明可影响众多生化过程。从肝细胞膜制备的IPG，在灌注到注射了Fura-2-葡聚糖的大鼠肝细胞上时，能迅速抑制去氧肾上腺素或血管加压素诱导的[Ca2+]i振荡。一种针对IPG的抗体可抑制胰岛素对[Ca2+]i振荡的抑制作用。通过细胞外Mn2+对细胞质Fura-2的淬灭速率测量表明，在未受刺激的细胞中Ca2+持续内流，且不受去氧肾上腺素或血管加压素影响。具体而言，IPG几乎完全消除了Mn2+淬灭速率。细胞外[Ca2+]升高可逆转IPG对[Ca2+]i振荡的抑制作用。我们得出结论，IPG通过减少维持[Ca2+]i振荡所需的持续Ca2+内流来抑制肝细胞Ca2+振荡。
